Snakebite In Australia Research Articles

Immunoreactivity of eastern small eyed snake (Cryptophis nigrescens) venom towards species-specific antibodies of five medically important venomous Australian elapids.

The eastern small eyed snake (Cryptophis nigrescens; CN) is an uncommon cause of snakebite in Australia despite the widespread distribution of the snake along the east coast of Australia. Diagnosis of envenomation relies on identification of the snake which is often not possible with animal snakebite cases. This study examined the immunoreactivity profile of CN venom towards specific rabbit IgG made against the medically relevant snake venom immunotypes found in Australia (tiger, brown, black, death adder and taipan). A simultaneous sandwich ELISA format was used to quantify CN venom binding to venom specific Protein A purified rabbit IgG. The binding profiles demonstrated weak binding of CN venom to rabbit IgG made against both tiger (N. scutatus) and black snake (P. australis) venoms with approximately 0.19% and 0.069% cross reactivity, respectively. However, the concentration of venom likely to be present in the urine of CN envenomed patients and the low cross reactivity suggest that envenomed veterinary patients are unlikely to be detected in the commercial snake venom detection kit. It is possible that CN envenomation is more common but may be underdiagnosed where snake venom antigen detection is relied upon solely. Serum biochemical abnormalities also overlap with other snake species found in the same geographical area. In respect of antivenom therapy, administration of tiger snake antivenom is supported by the binding data, but due to the low cross reactivity multiple vials may be required. Limited clinical evidence also supports the efficacy of tiger snake antivenom for envenomation by CN.

Harm due to the use of pressure bandage immobilisation in patients bitten by snakes in Australia

Background Pressure bandage immobilisation has remained the recommended first aid treatment for more than 40 years in Australia. However, whilst it is used in most people bitten by a snake, it is often applied poorly, and patients have been envenomed despite good pressure bandage immobilisation. We report two patients who suffered harm from this procedure. Case reports Two men, a 35-year-old and a 44-year-old, were bitten by snakes. Both had a prompt application of pressure bandage immobilisation, and both reported significant pain requiring opioid analgesia whilst being transferred from remote Australia to Cairns Hospital, Queensland. There were substantial delays (9.5 h and 7.5 h) before the pressure bandage immobilisation was released. As a result, both patients developed severe rhabdomyolysis (33,600 U/L and 16,800 U/L [normal < 171 U/L], respectively); there was no evidence of systemic envenoming. The 35-year-old developed a compartment syndrome that required urgent and repeated surgery. The 44-year-old has ongoing foot paraesthesia two years after the bite. Conclusion With limited good evidence of benefit, and many issues with its use, I recommend that pressure bandage immobilisation as a first aid measure for snakebite in Australia needs to be re-examined.

D-dimer testing for early detection of venom-induced consumption coagulopathy after snakebite in Australia (ASP-29).

ObjectiveTo assess the accuracy and marginal value of quantitative D‐dimer testing for diagnosing venom‐induced consumption coagulopathy (VICC) in people bitten by Australian snakes.Design, settingAnalysis of data for suspected and confirmed cases of snakebite collected prospectively by the Australian Snakebite Project, 2005–2019, from 200 hospitals across Australia.Participants1363 patients for whom D‐dimer was quantitatively assessed within 24 hours of suspected or confirmed snakebite.Main outcome measuresDiagnostic performance of quantitative D‐dimer testing for detecting systemic envenoming with VICC (area under the receiver operating characteristic curve, AUC); optimal D‐dimer cut‐off value (maximum sum of sensitivity and specificity).ResultsD‐dimer values exceeded 2.5 mg/L within three hours of the bite for 95% of patients who developed VICC, and were lower than 2.5 mg/L for 95% of non‐envenomed patients up to six hours after snakebite. The AUC for diagnosing envenoming with VICC on the basis of quantitative D‐dimer testing within six hours of snakebite was 0.97 (95% CI, 0.96–0.98; 944 patients). Diagnostic performance increased during the first three hours after snakebite; for quantitative D‐dimer testing at 2–6 hours, the AUC was 0.99 (95% CI, 0.99–1.0); with a cut‐off of 2.5 mg/L, sensitivity was 97.1% (95% CI, 95.0–98.3%) and specificity 99.0% (95% CI, 97.6–99.6%) for VICC. For 36 patients with normal international normalised ratio (INR) and activated partial thromboplastin time (aPTT) values 2–6 hours after snakebite, the AUC was 0.97 (95% CI, 0.93–1.0); with a cut‐off of 1.4 mg/L, sensitivity was 94% (95% CI, 82–99%) and specificity 96% (95% CI, 94–97%). In all but one of 84 patients who developed VICC‐related acute kidney injury, D‐dimer values exceeded 4 mg/L within 24 hours of the bite.ConclusionD‐dimer concentrations assessed 2–6 hours after snakebite, with a cut‐off value of 2.5 mg/L, could be useful for diagnosing envenoming with VICC.

Incidence of fatal snake bite in Australia: A coronial based retrospective study (2000–2016)

IntroductionIt has been over 20 years since a national review of recorded deaths from snake envenoming. The present study aimed to provide an updated review of the epidemiology of deaths from snake bites in Australia. MethodsDeaths were identified from January 2000 to December 2016 from the National Coronial Information System. Cases identified due to snakes were extracted with data on coronial findings, autopsy and police records. ResultsThirty five deaths (2.2 per year) were ascribed or antecedent to a snake bite. Sixteen cases were attributed to snake bite/envenoming as leading directly to death, with other direct causes of death being multiple organ failure (n = 3), intracerebral haemorrhage (n = 2), cerebral hypoxia or anoxia (n = 3), cardiac arrest (n = 1), complications of snake bite (n = 3) or brain stem death (n = 1). Four cases did not have a snake bite indicated in the case history, with an initial diagnosis of either hyperthermia, stroke, gastroenteritis and a horse accident. The median age was 46.5 years (range 1.5–70 years), and 74% were males (n = 25). The time from bite to death varied from 1 h to 19 days. Fifty four percent of bites occurred at the person's residence (n = 1), with 17 being in an urban environment. ConclusionsDeath from snake bite remains rare in Australia, and has maintained a steady rate for over 20 years. Usually considered a ‘rural issue’, and with varying recorded causes of death, a nationally co-ordinated effort to further review the national picture of envenoming in Australia can inform education and resource needs within state and local contexts.

Snakebite in Australia: a practical approach to diagnosis and treatment

Snakebite is a potential medical emergency and must receive high-priority assessment and treatment, even in patients who initially appear well. Patients should be treated in hospitals with onsite laboratory facilities, appropriate antivenom stocks and a clinician capable of treating complications such as anaphylaxis. All patients with suspected snakebite should be admitted to a suitable clinical unit, such as an emergency short-stay unit, for at least 12 hours after the bite. Serial blood testing (activated partial thromboplastin time, international normalised ratio and creatine kinase level) and neurological examinations should be done for all patients. Most snakebites will not result in significant envenoming and do not require antivenom. Antivenom should be administered as soon as there is evidence of envenoming. Evidence of systemic envenoming includes venom-induced consumption coagulopathy, sudden collapse, myotoxicity, neurotoxicity, thrombotic microangiopathy and renal impairment. Venomous snake groups each cause a characteristic clinical syndrome, which can be used in combination with local geographical distribution information to determine the probable snake involved and appropriate antivenom to use. The Snake Venom Detection Kit may assist in regions where the range of possible snakes is too broad to allow the use of monovalent antivenoms. When the snake identification remains unclear, two monovalent antivenoms (eg, brown snake and tiger snake antivenom) that cover possible snakes, or a polyvalent antivenom, can be used. One vial of the relevant antivenom is sufficient to bind all circulating venom. However, recovery may be delayed as many clinical and laboratory effects of venom are not immediately reversible. For expert advice on envenoming, contact the National Poisons Information Centre on 13 11 26.

Treatment of snakebite in Australia: gathering the evidence

[Extract] The World Health Organization has declared snakebite a neglected tropical disease. Although Australia has many of the world's most venomous snakes, the annual rate of envenoming here is much lower than in some other regions. In Australia, rates of snakebite are higher in tropical areas — a prospective study in the Northern Territory estimated the rate of envenoming to be 7.6 per 100 000 people per year. Sadly, there were at least three snakebite deaths in Queensland in the summer of 2012–2013.

Toxinology in Australia's colonial era: A chronology and perspective of human envenomation in 19th century Australia

The medical management of those envenomed by snakes, spiders and poisonous fish in Australia featured extensively in the writings 19th century doctors, expeditioners and anthropologists. Against the background of this introduced medical doctrine there already existed an extensive tradition of Aboriginal medical lore; techniques of heat treatment, suction, incision and the application of plant-derived pharmacological substances featured extensively in the management of envenomed victims. The application of a hair-string or grass-string ligature, suctioning of the bite-site and incision were practised in a variety of combinations. Such evolved independently of and pre-dated such practices, which were promoted extensively by immigrant European doctors in the late 19th century. Pacific scientific toxinology began in the 17th century with Don Diego de Prado y Tovar's 1606 account of ciguatera. By the end of the 19th century more than 30 papers and books had defined the natural history of Australian elapid poisoning. The medical management of snakebite in Australia was the focus of great controversy from 1860 to 1900. Dogmatic claims of the supposed antidote efficacy of intravenous ammonia by Professor G.B. Halford, and that of strychnine by Dr. Augustus Mueller, claimed mainstream medical attention. This era of potential iatrogenic disaster and dogma was brought to a conclusion by the objective experiments of Joseph Lauterer and Thomas Lane Bancroft in 1890 in Brisbane; and by those of C.J. Martin (from 1893) and Frank Tidswell (from 1898), both of Sydney. The modern era of Australian toxinology developed as a direct consequence of Calmette's discovery, in Paris in 1894, of immune serum, which was protective against snakebite. We review the key contributors and discoveries of toxinology in colonial Australia.

Treatment of snakebite in Australia: The current evidence base and questions requiring collaborative multicentre prospective studies

Despite the wealth of anecdotes and case reports there are fundamental questions of management of snakebite in Australia that remain unresolved or for which the current evidence is limited. The efficacy in the field, potential limitations and possibility of improvements in pressure immobilisation first aid need objective studies in humans. Optimal bandage sizes, stretch and pressure for different sized limbs need further evaluation, as does the use of pressure pads. Better definitions of specific clinical envenoming syndromes attributable to individual snake species are required, including elucidation of within-genus variations, similarities and differences. Venom studies suggest this is especially important for species within the brown snake ( Pseudonaja) and death adder ( Acanthophis) genera. Appropriate antivenom types, doses and dosing intervals for individual snake species should be more formally studied in patients. Especially important are confirmation of the need for higher doses of brown snake antivenom, while possibly limiting unnecessarily high doses, confirmation of the critical importance of early antivenom use to prevent pre-synaptic neurotoxicity in Taipan and tiger snake bites and ascertainment of whether larger doses of antivenom are unhelpful in Taipan bites after specified time delays. Confirmation of clinical efficacy and dosing recommendations for use of tiger snake ( Notechis) antivenom in envenoming from Australian copperhead ( Austrelaps spp.), broad headed ( Hoplocephalus spp.) and rough-scaled snakes ( Tropidechis carinatus) also require formal study in patients. Other examples of clinical relevance of cross-specificity of current and future monospecific antivenoms and whether there are geographical variations in antivenom responses within species will require elucidation. Prospective multicentre collaborative studies with predefined data collection and serial venom level assays are proposed as the way forward in Australia to help resolve therapeutic uncertainties and to establish a firmer evidence base for best-practice treatment guidelines for Australasian elapid snakebite.

Molecular Diversity in Venom from the Australian Brown Snake, Pseudonaja textilis

Venom from the Australian elapid Pseudonaja textilis (Common or Eastern Brown snake), is the second most toxic snake venom known and is the most common cause of death from snake bite in Australia. This venom is known to contain a prothrombin activator complex, serine proteinase inhibitors, various phospholipase A2s, and pre- and postsynaptic neurotoxins. In this study, we performed a proteomic identification of the venom using two-dimensional gel electrophoresis, mass spectrometry, and de novo peptide sequencing. We identified most of the venom proteins including proteins previously not known to be present in the venom. In addition, we used immunoblotting and post-translational modification-specific enzyme stains and antibodies that reveal the complexity and regional diversity of the venom. Modifications observed include phosphorylation, gamma-carboxylation, and glycosylation. Glycoproteins were further characterized by enzymatic deglycosylation and by lectin binding specificity. The venom contains an abundance of glycoproteins with N-linked sugars that include glucose/mannose, N-acetylgalactosamine, N-acetylglucosamine, and sialic acids. Additionally there are multiple isoforms of mammalian coagulation factors that comprise a significant proportion of the venom. Indeed two of the identified proteins, a procoagulant and a plasmin inhibitor, are currently in development as human therapeutic agents.

Snakebite in Australia: The role of the Venom Detection Kit

Snakebite in Australia: The role of the Venom Detection Kit

Snake bite in Australia: first aid and envenomation management

Australia is inhabited by a large variety of snakes, including some of the most poisonous in the world. Sightings are regular, and the incidence of snake bite is estimated to be several thousand a year. A bite does not necessarily result in envenomation occurring, however there are at least 300 snakebites a year requiring treatment of envenomation, with between 1 and 4 fatalities every year. The incidence of fatalities from snake bite has increased over recent years. The explanation for this is unclear, but possible reasons include the urban sprawl, and a delay in application of appropriate first aid and definitive treatment for envenomation. Emergency nurses in particular should be aware of the first aid techniques appropriate for Australian snake bite, as well as the recognition and management of envenomation. This article will outline the steps required and rationale for applying first aid techniques considered to be effective in retarding spread and circulation of snake venom. It will also discuss the manifestations that indicate systemic envenomation, and management considered to be responsible for reducing the incidence of death from snake envenomation in Australia.

Fatal snakebite in Australia.

More than 20 venomous snakes found in Australia belong to the family Elapidae . Although their venom delivery system is less efficient than that of the Viperidae , their venoms are extremely potent. The active components of Australian elapid venoms include neurotoxins, myotoxins , hemolysins, and factors producing hypocoagulability. The groups at particular risk of snakebite are children, agricultural workers, bushwalkers , and herpetologists . A high index of suspicion must be maintained when investigating cases of sudden unexpected death in these groups. The bite wound itself may be particularly easily overlooked as there is little local reaction to many elapid bites. The necropsy findings in fatalities are predictable from the known properties of the venoms of the various species. However, these findings are non-specific and the diagnosis ultimately rests upon the demonstration of the presence of venom by immunoassay. For this purpose swabs from the bite site, the overlying clothing, the excised bite site, the local and regional lymph nodes, urine, and blood may be used.

Snake bite in Australia--the problems involved and a protocol for hospital management.

Despite a great deal of original research into Australian snakes and their complex venoms, there is still confusion about the correct first-aid and hospital management of the bitten patient. This review illustrates the difficulties in diagnosis and treatment and presents a well tried protocol for the successful management of snake bite.